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4. To what extent are people exposed to phthalates?

    The SCHER opinion states:

    The diet, particularly fatty food, is responsible for most
                                        of the DEHP exposure in adults.
    The diet, particularly fatty food, is responsible for most of the DEHP exposure in adults.
    Source: Steve Woods

    3.4. New information on exposure and toxicity of phthalates

    SCHER has no information on use patterns, occurrence, and human exposures to diisodecyl (DIDP) and di-n-octyl phthalate (DNOP). For DEHP, DINP, DIBP, DNBP, and DBP, a large number of studies relevant to exposure and risk assessment of phthalates are available including recent risk assessment reports (RAR). Therefore, the following text only gives short summaries.

    3.4.1 Exposure assessment

    Detailed exposure assessment using concentrations of phthalates in food, environmental media and materials including predictions by modelling have been performed in the EU- RARs. For an additional detailed overview on occurrence of phthalates and assessments of human exposures, see Heudorf et al., 2007.

    Conservative exposure assessments for DEHP, DINP, DIBP, DNBP, and DBP are given in the available RARs. However, more recent studies derived human exposures to phthalates by biomonitoring of metabolite excretion since this results in a more precise estimate of average exposures and the range of exposures as compared to exposure estimates based on concentrations of phthalates in environmental media and food and assumptions on uptake of these media. The linear two-compartment model published by Kohn et al. (2000) and David (2000) based on the creatinine adjusted concentrations of phthalate ester metabolites in urine and the molar fraction of the urinary excreted metabolite related to the parent compound (Koch et al. 2004a) were used to derive estimates of phthalate exposure in children (Table 1). If available, results for adults are presented for comparison.

    The most representative biomonitoring data from two surveys are available on DEHP. Within the US-National Health and Nutritition Examination Survey (NHANES) 2001-2002, information of urinary levels of phthalate metabolites were collected from 2782 participants aged 6 years and older (NCEH 2005). In the pilot study for the German Environmental Survey on Children (GerES IV), urinary levels of phthalates were determined in random urine sample of 254 children aged 3 to 14 years (Becker et al. 2004). In comparison to the NHANES subpopulation of children aged 6 to 11 years, the median levels of DEHP metabolites were slightly higher in the German samples, while the 95th percentiles were lower. In the German sample, the concentrations of secondary metabolites in urine were increased in boys as compared to girls and were significantly higher in children aged 6-7 years compared to children in the age group 13-14 years.

    Measured urinary concentrations for different phthalates

    While in NHANES, no differences with respect to ethnicity were found, an association with ethnicity was observed in two other US studies. In an investigation of 90 girls from 4 US sites representing four racial/ethnic groups, exposure was found to depend on ethnicity with lowest concentrations observed for whites and on study site with differences of factor 1.7 (Wolff et al. 2007). These results were supported by Teitelbaum et al (2008) who observed a very high exposure to phthalates in 35 healthy Hispanic and black children.

    Overall, it has to be considered that the knowledge of the toxicokinetic behaviour of DEHP and other phthalates in humans is still limited and age related differences have not been sufficiently evaluated. Despite these uncertainties, the average exposure of children is approximately twofold higher than that of adults. Different life style factors, eating behaviours, a higher dietary intake compared to body weight and the ingestion of dust from indoor surfaces may play a role. In a recent study from Germany, both urine samples and food duplicates were collected from 5-8 year old boys over 3 consecutive days (Heger 2007). The results indicated that diet (without beverages) was responsible for about 50 % of the exposure derived from biomonitoring (1.4 µg/kg b.w. vs. 3.1 µg/kg b.w.). Thus, other important sources, which are not yet identified, must exist. For adults, DEHP exposure is dominated by the dietary intake (Fromme et al. 2007), particularly from fatty foods.

    Moreover, it has to be noted that using a scenario-based indirect approach no differences between adults and children 4-10 years old could be observed but a clearly increased exposure was calculated for children less than 4 years of age (Wormuth et al. 2006).

    Since DINP replaces DEHP in many applications, an increase in the exposure to DINP occurs. Between 1999 and 2004, the proportion of DEHP to total phthalate usage decreased from 42% to 22% and the proportion of DINP and DIDP (no data specifically on DINP are available) increased from 35% to 58% (ECPI 2006). Beyond this, Wittassek et al. (2007) quantified the exposure to phthalate in 20-29 year old students from 1988 to 2003 in a retrospective study in Germany. A continuous decrease in DEHP exposure was observed from 1996 until 2003 with an increase in DINP (Median: 0.2 µg/kg b.w. to0.4 µg/kg b.w.) exposure. At present, biomonitoring data on the metabolites of DINP or other phthalates in children are not available for exposure assessment and are needed.

    DINP intake for children aged 3-12 months and 13-26 months was assessed by migration data and average mouthing times using statistical modelling (US-CPSC, 1998).Migration rates were developed from in-vitro experiments and scaled. These data were combined into an analytical model that used a lognormal distribution for human exposure duration, combining estimates from the separate experiments. The results showed a geometric mean average daily intake of 5.7 μg/child/day (95% confidence interval of 2.5 to 12.9) for children between ages 3 and 12 months (less then 1 μg/kg bw/day for an 8 kg child). The distribution was very skewed, with an estimate of 5% of children at an intake of 94.3 μg/child/day (more than 10 μg/kg bw/day for an 8 kg child) or more (95% confidence interval 50.1 to 225.6). The values for children at 13-26 months were considerably lower with a geometric mean of less than 1 µg/child/per day.

    In conclusion, the exposure data based on biomonitoring indicate that average exposures are well below the TDI for DEHP, but the DEHP body burden may approach or even exceed the TDI in some highly exposed groups of population. For the other phthalates studied, the 95th percentile exposures derived are below the TDIs except for DNBP. For DNBP, a significant part of the population may be exposed to doses above the TDI indicating a need for further reductions in exposures.

    Source & ©: SCHER   Opinion on phthalates in school supplies (2008),
    3.4. New information on exposure and toxicity of phthalates, p. 9 – 13

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